Guillain-Barré Syndrome and Posterior Reversible Encephalopathy Syndrome following Spinal Surgery

Guillain-Barré syndrome (GBS) typically occurs after gastroenteritis and respiratory tract infec-tion, but surgery has also been considered one of the triggers. Posterior reversible encepha-lopathy syndrome (PRES) is a rare complication of GBS. A normotensive female in her 70s pre-sented ascending paralysis and frontal-parieto-occipital subcortical lesions with intermittent hypertension after spinal surgery. Nerve conduction studies revealed demyelinating polyneu-ropathy. The patient’s brain lesions disappeared with amelioration of hypertension. She was diagnosed with the demyelinating form of GBS and PRES caused by intermittent hypertension. Intravenous immunoglobulin G (IVIG) improved her symptoms without exacerbation of the PRES. Surgery can be a trigger of GBS, and GBS can cause PRES by hypertension and present as central nervous lesions. It is important to treat hypertension before using IVIG when PRES is suspected as a complication of GBS, since the encephalopathy can be exacerbated by IVIG. There may be more undiagnosed cases of the coexistence of GBS and PRES after surgery be-cause surgery itself can also cause PRES. Proper control of blood pressure and confirmation of negative central nervous lesions are required to treat GBS patients with IVIG safely

Focal brain lactate accumulation in metformin-induced encephalopathy without systemic lactic acidosis: A case report suggesting mitochondrial vulnerability in lentiform fork sign

Metformin causes metabolic encephalopathy in some patients with end-stage chronic kidney disease, resulting in impaired consciousness and parkinsonism. This encephalopathy has a very characteristic magnetic resonance imaging feature in lentiform nuclei known as the “lentiform fork sign”. However, the mechanism is unknown. Here, we report a case of metformin-induced encephalopathy with a novel observation of lactate accumulation in the lentiform nuclei on magnetic resonance spectroscopy without systemic lactic acidosis. Since metformin is an inhibitor of mitochondrial complex-I, this focal brain lactate accumulation implies that a part of the pathogenesis of metformin-induced encephalopathy is the focal vulnerability of mitochondria to metformin in the lentiform nuclei. When metformin causes encephalopathy, not only testing for serum lactic acidosis and performing routine magnetic resonance imaging but also evaluation of brain lactate accumulation by magnetic resonance spectroscopy should be required to elucidate the etiology

Focal brain lactate accumulation in metformin-induced encephalopathy without systemic lactic acidosis: A case report suggesting mitochondrial vulnerability in lentiform fork sign

Metformin causes metabolic encephalopathy in some patients with end-stage chronic kidney disease, resulting in impaired consciousness and parkinsonism. This encephalopathy has a very characteristic magnetic resonance imaging feature in lentiform nuclei known as the “lentiform fork sign”. However, the mechanism is unknown. Here, we report a case of metformin-induced encephalopathy with a novel observation of lactate accumulation in the lentiform nuclei on magnetic resonance spectroscopy without systemic lactic acidosis. Since metformin is an inhibitor of mitochondrial complex-I, this focal brain lactate accumulation implies that a part of the pathogenesis of metformin-induced encephalopathy is the focal vulnerability of mitochondria to metformin in the lentiform nuclei. When metformin causes encephalopathy, not only testing for serum lactic acidosis and performing routine magnetic resonance imaging but also evaluation of brain lactate accumulation by magnetic resonance spectroscopy should be required to elucidate the etiology

Alternative to steroid therapy for myasthenia gravis and myositis occurring as immune‐related adverse events

This is the peer reviewed version of the following article: Kamada, S., Hanazono, A., Sanpei, Y., Inoue, T., Suzuki, S., Sugawara, M. and Iijima, K. (2019), Alternative to steroid therapy for myasthenia gravis and myositis occurring as immune-related adverse events. Clin Exp Neuroimmunol, 10: 190-191,which has been published in final form at https://doi.org/10.1111/cen3.12526. This article may be used for non-commercial purposes in accordancewith Wiley Terms and Conditions for Use of Self-Archived Versions